UV-induced tumors express multiple tumor-associated antigens which under varying conditions can selectively activate either suppressor or effector pathways of immune response. We are studying this model, using both monoclonal antibodies and Il-2-dependent continuous T-cell lines, with the aim of identifying the different tumor specific antigens and determining the mechanisms by which these antigens activate different antitumor responses. Our progress to date includes the generation and characterization of UV-1, a continuous T suppressor cell line with in vivo and in vitro activity. We believe UV-1 represents the suppressor cells induced by UV irradiation of mice. We have also generated several monoclonal antibodies reactive with UV tumors. These lines are presently in bulk culture and will be cloned. Investigations into the mechanisms of how UV radiation generates tumor-specific suppression has resulted in several new findings. First, by transplantation criteria, it appears that UV irradiated skin expresses neoantigens that are cross reactive with UV-induced tumors. We intend to establish a more formal link between UV irradiated skin and skin tumors by investigating if the antitumor monoclonal antibodies are reactive with both tissues. Second, a new phenomenon we term "phototolerance" has been described. That is, when antigen (purified human IgG) is introduced into a host through a UV-irradiated skin site, the host is specifically unresponsive at the cellular and humoral level to subsequent challenge with antigen. Further work on phototolerance is planned with the objective of determining the range of antigens to which the phenomenon holds. Clearly, the capacity to induce tolerance to any protein antigen, including transplantation antigens, is important.